Vagus nerve stimulation attenuates myocardial ischemia/reperfusion injury by inhibiting the expression of interleukin-17A

Yi,Chunfeng; Zhang,Changjiang; Hu,Xiaorong; Li,Yuanhong; Jiang,Hong; Xu,Weipan; Lu,Jiajia; Liao,Yuanxi; Ma,Ruisong; Li,Xuefei; Wang,Jichun

doi:10.3892/etm.2015.2880

Vagus nerve stimulation attenuates myocardial ischemia/reperfusion injury by inhibiting the expression of interleukin-17A

Authors:
- Chunfeng Yi
- Changjiang Zhang
- Xiaorong Hu
- Yuanhong Li
- Hong Jiang
- Weipan Xu
- Jiajia Lu
- Yuanxi Liao
- Ruisong Ma
- Xuefei Li
- Jichun Wang
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Affiliations: Department of Cardiology, Renmin Hospital of Wuhan University, Cardiovascular Research Institute of Wuhan University, Wuhan, Hubei 430060, P.R. China, Department of Cardiology, Central Hospital of Enshi Tujia and Miao Autonomous Prefecture, Enshi, Hubei 445000, P.R. China
Published online on: November 18, 2015 https://doi.org/10.3892/etm.2015.2880
Pages: 171-176

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Abstract

Interleukin (IL)-17A has an important role in myocardial ischemia/reperfusion (I/R) injury, and vagal stimulation (VS) has been demonstrated to exert cardioprotective effects. The present study aimed to investigate the effects of VS on a rat model of myocardial I/R injury, and detected an association between VS and IL‑17A. Anesthetized rats underwent VS (2 msec; 10 Hz) or were treated with anti‑IL‑17A neutralized monoclonal antibodies (mAbs) (200 µg; iv), and subjected to ischemia for 30 min prior to 4 h reperfusion. The following parameters were measured: Infarct size; lactate dehydrogenase (LDH), creatine kinase (CK), malondialdehyde (MDA), superoxide dismutase (SOD) and caspase‑3 activity levels; tumor necrosis factor (TNF)‑α and IL‑6 expression levels; and the percentage of terminal deoxynucleotidyl-transferase mediated dUTP nick‑end labeling (TUNEL) positive cells. High mobility group box 1 protein (HMGB1) and IL‑17A expression levels were assessed by immunoblotting. Following 4 h reperfusion, VS was able to significantly decrease the infarct size and the activity levels of LDH and CK (P<0.05). Furthermore, VS administration significantly suppressed the increased MDA and decreased SOD activity levels, and significantly reduced caspase‑3 activity and the percentage of TUNEL‑positive cells (P<0.05). Treatment with anti‑IL‑17A mAbs demonstrated the same effects as VS. Furthermore, VS was able to significantly inhibit the increased expression levels of TNF‑α, IL‑6, HMGB1 and IL‑17A induced by I/R (P<0.05). The results of the present study suggested that VS may attenuate myocardial I/R injury by reducing the expression of inflammatory cytokines, oxidative stress and the apoptosis of cardiomyocytes. Furthermore, VS may induce cardioprotective effects, which may be associated with the inhibition of IL-17A expression.

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